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首页> 外文期刊>Cytokine >Loss of STAT3 in mouse embryonic fibroblasts reveals its Janus-like actions on mitochondrial function and cell viability
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Loss of STAT3 in mouse embryonic fibroblasts reveals its Janus-like actions on mitochondrial function and cell viability

机译：小鼠胚胎成纤维细胞中STAT3的丢失揭示了其对线粒体功能和细胞活力的似Janus的作用

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摘要

STAT3 has been implicated in mitochondrial function; however, the physiological relevance of this action is not established. Here we studied the importance of STAT3 to the cellular response to stimuli, TNFα and serum deprivation, which increase mitochondrial reactive oxygen species (ROS) formation. Experiments were performed using wild type (WT) and STAT3 knockout (KO) mouse embryonic fibroblasts (MEF). Both WT and STAT3 KO MEF expressed similar levels of tumor necrosis factor receptor 1 (TNFR1) and exhibited comparable IκBα degradation with TNFα. However, in the absence of STAT3 nuclear accumulation of NFκB p65 with TNFα was attenuated and induction of the survival protein c-FLIPL was eliminated. Nonetheless, WT MEF were more sensitive to TNFα-induced death which was attributed to necrosis. Deletion of STAT3 decreased ROS formation induced by TNFα and serum deprivation. STAT3 deletion was associated with lower levels of complex I and rates of respiration. Relative to WT cells, mitochondria of STAT3 KO cells released significantly more cytochrome c in response to oxidative stress and had greater caspase 3 cleavage due to serum deprivation. Our findings are consistent with STAT3 being important for mitochondrial function and cell viability by ensuring mitochondrial integrity and the expression of pro-survival genes.
机译：STAT3与线粒体功能有关。然而，该作用的生理相关性尚未建立。在这里，我们研究了STAT3对细胞对刺激，TNFα和血清剥夺的反应的重要性，这会增加线粒体活性氧（ROS）的形成。实验是使用野生型（WT）和STAT3敲除（KO）小鼠胚胎成纤维细胞（MEF）进行的。 WT和STAT3 KO MEF均表达相似水平的肿瘤坏死因子受体1（TNFR1），并表现出与TNFα相当的IκBα降解。但是，在没有STAT3的情况下，NFκBp65和TNFα的核积累被减弱，存活蛋白c-FLIPL的诱导被消除。尽管如此，WT MEF对TNFα引起的死亡（由于坏死）更为敏感。 STAT3的删除减少了TNFα诱导的ROS形成和血清剥夺。 STAT3缺失与复杂I水平和呼吸频率降低相关。相对于WT细胞，STAT3 KO细胞的线粒体响应氧化应激而释放出更多的细胞色素c，并且由于血清剥夺而具有更大的caspase 3裂解。我们的发现与STAT3通过确保线粒体的完整性和促存活基因的表达对于线粒体功能和细胞生存力至关重要有关。

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